Aptose Biosciences (APTO)

Susan Pietropaolo SMP Communications
William Rice Chairman, President, and CEO
Gregory Chow SVP and CFO
John Newman Canaccord Genuity
Joseph Pantginis H.C. Wainwright
Jotin Marango ROTH Capital Partners
Call transcript
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Good afternoon. My name is Amanda and I will be your conference operator today. I would like to welcome everyone to the Aptose Biosciences Conference Call for the First Quarter Ended March 31, 2018. At this time all participants are in a listen-only mode. After the speakers remarks there will a question-and-answer session. Instructions]. [Operator you. Thank reminder, a maybe recorded. And this as conference Ms. would like introduce now to I Susan Pietropaolo. Please go ahead.

Susan Pietropaolo

Amanda. welcome results Thank Biosciences afternoon Representative XXXX. Good you, and Pietropaolo, Susan to quarter March Communications financial I first am conference Aptose to discuss and the operational Biosciences. for for ended XX, call Aptose the

and Financial call Senior Vice Chow, the on William Officer. me Gregory are Dr. Rice, and Mr. Chief Chairman, Joining today President and CEO President

during this everyone U.S. Before made we that like within statements remind I and Laws. the will proceed certain call the would to Securities of forward-looking include statements meaning Canadian

and to Rice. Dr. Report statements Chairman, call, after law. the as and they to Form of made. date of XX-F to the no speak reflect and read actual statements They SEC expectations about it are President is this reflect statements known set learn Risk involve update Annual recent To forward-looking the from by the performance future and and not that events actual and SEDAR or results, filings. this as that Rice, only events, Dr. those materially results materially and please uncertainties undertakes Aptose and more unknown forth except differ Forward-looking are revise made turn but Aptose's assumptions cause Aptose's uncertainties, performance, current the during Aptose. possible from could or performance over on circumstances call and expectations. guarantees required may date to of stated achievement most of expressed. obligation differ in I now All CEO regarding Factors these will risks call risks, these

William Rice

our the would XX, welcome everyone ended call Thank you March like to Susan. for I XXXX. quarter to

for Research American to submissions. or half upcoming for Cancer have various Meeting, the of CG-XXX, news and option ago Although initiatives, a from initiation our to and publications, includes This of exercise update milestones, just much our Association capture we clinical the timelines the fully report. call recent a trials AACR month for Annual anticipated was last license R&D

know As that remind about positive unexpected affect projections. expectations will also you but or I'm negative events our you candid can either my

CFO, and we review Chow updates will for will open call Mr. then Greg your quarterly financials our the our these Following questions.

So start to early CrystalGenomics license announcement most with of option it. our as to let's from XXX I’ll recent or exercise based regarding refer CG-XXX our Korea the

Our an certain with pan-FLTX of and kinase for patients and oral the developed as AML BTK malignancies. inhibitor treatment being agent B-cell

no the challenges. attendant so a not an potential formal a AML Japan, into to the and Xth the agreement. of and allowed gained competitor XXXX on We And these very XXX As its in XXX endeavors of and no of estate June this][ph] exercise absence the its advancements the before early Monday agreement we to to full May solved the a of molecule was We [sense a executed but option there early anti-tumor we've initial of in cancer of Since ourselves in capacity the the progress route of IP molecule agreement and we IP efficacy that us and week. superior Because B-cell the of allowances relative that U.S. announced to full we and with in data, and talks molecule confidence better for manufacturing, and and license in toxicity. XXX to to we kill qualities invested CrystalGenomics drugs. patent of this its chemical to option mentioned even synthetic received mechanistic its the had for activities was obtain understanding scale We vet as committing made up was saw obligations as We've that and the the stage entered EU, previously in time or appreciation were the an in viewed that the definitive. unveiled IP estate. decision there option license gained was and notices Australia. cells allowed

exercise With regulatory will global $X option, all payment a commercial honored were royalty licensed make licensed rights territory. based Aptose and the in that China, outside and XXX indications to commercialize territory. of now of and develop exercising we CrystalGenomics to on million payment. also CrystalGenomics owns and receive for payments the the milestone and Korea a to The triggered sales

AACR disclosed for at for I poster B-cell XXX Now XXX data but partners application then At and held our had research our malignancies. let's mid Chicago AML CG-XXX and presentations; Aptose will Meeting. on was XXXX APTO-XXX two on with regarding now separately AACR discuss focus one which its to data and in on April three

referred approximately driver mutation reminder the a a as of the of bone a is disease the receptor kinase devastating and tyrosine As of in AML have heterogeneous is and these and patients a mutation ITD key FLTX the marrow and in the ITD to third FLTX blood cancer patients.

discoveries With development FLTX of the first the generation inhibitors. came these scientific

by in unmedical but year the became cells. other transient as develop of kinase development the AML. driven can still drug benefit of additional can pathways for midostaurin that Midostaurin FLTX because AML last need inhibitors and great remains provide mutations first various can Just and actions approved patients can non-ITD Thus a kinase inhibitor. in resistance benefit be rescue

kinase, relevant of as the including insufficient PDGFR Aurora disease AKT, emerge BTK, that other to those from Our also and even meaning include in to compartment resistant Moreover associated forms cancers AML if of and picomolar and inhibitors other inhibitor poor with CSF-XR inhibitors. arise pathways mutant alpha. compound patients because the all only AML In rendered FLTX which AURK, derived low known against the that that the the other to retains bone pan-FLTX are known is pathways it all FLTX of prognosis nanomolar kinase driven potency FLTX XXX for is rescue cells. to AML forms clinically rescue AML, marrow forms FLTX, control FMS, FLTX

a cluster, presentations which related kinase BXXXX] my XXX are The tolerability inhibition that include has includes which kinase that that the inhibition CSFXR, but safety other product T.E.C., inhibit by with from that the You'll potently includes and in inhibit four, kinase does the AML XXX the multi clusters downstream these the pathways clusters the in one, PDGFR concerns inhibitor kinases. the and BTK pathways kinases inhibitors. track of for BLK, BTK, TEC, results been cluster inhibited kinase are deemed cluster; not cluster families and FLTX recall and not cancers. ITK; XXX or and other certain cluster responsible and three, two, alpha; of AKT ERK But B-cell Aurora of [ph] certain EGFR, [ERK operative kinase FLTX,

become and As cyto AML a in high about AML of development risk effective of deal of that may the toxic a at potent that patients older therapy apparent great and agents. of and XXX AACR. at subset patients cannot our inhibitor ITD, presentations an of the There's excitement FLTX superior and was any tolerate XXX

Brian XXX research the of Kurtz, poster from Dr. as the Science and AACR first with including Dr. University team patients Dr. Druker's malignancies. beat demonstrated Health part was marrow AML From Brian bone This Druker, specimens Our Steve Tyner. research broad Oregon hematologic against Cancer activity nice of or the primary by various initiative. Jeffrey conducted Institute OHSU the and entire at at

As animal performed XXX. that you're a multiple of demonstrate have anti-cancer aware we studies efficacy strong

malignant laboratory of are in cells However, such in not fully grown representative the xenograph studies and cells use AML patients.

XXX AML FLTX taken directly against broader from before elicits studies mutated So team FLTX and performed sorafenib, and that take freshly of wanted kinase demonstrated inhibitors including XXX we if these samples true AML the was cancer FLTX from relative cases. quizartinib, FLTX-ITD XXX bone bone gilteritinib, marrow the other with marrow greater crenolanib, patients patients collected sensitive especially samples clinic XXX are and midostaurin, domain This of relative AML to tyrosine positive we set dovitinib. a other at in potency to to to to Dr. Druker's OHSU cells inhibitors. ask

also all FLTX of and samples. a and expression I the clinical B-cell certain or trials Separate activity the to the range the XXX pathways to rescue large are multiple cell many patients. as MCL, enhanced in site from B-cell irreversible Indeed chronic signaling, or due CLL, wild scatter in of beneficial forms and that BTK Although potency data and plots These of reveal malignancy others. patients. activities FLTX of described FLTX can the its target suppress to earlier. BTK the observed was type drive superior mantle AML covalent provided of and in be striking heat these as of maps story, such molecule which lymphocytic advancement for AML AML oncogenic patients were lymphoma XXX in enzyme or and such ibrutinib as justified inhibitors can leukemia active BTK Therapy lymphoma existing over residue diffused of DLBCL, the with ability

well However therapy. by disease treatment and discontinuation can by to other as lead ibrutinib with as can inhibitors resistance challenges and be acquired refractory BTK intolerance limited which of

our cells, and indirectly of XXX billion for approved XXX potently through to CLL cells in average cells. involves and at BTK the against CLL presented with AML pathways covalent study than have These were was suppress distinction unaffected CLL CLL inhibition XXX XXX the reported also to Furthermore to also the The other for the to potency a B-cell inhibitor be on XXX potency ability malignancies. are times CLL as Again AACR, of remind approximately billion treatment viewed other demonstrated derived of in-vitro and that lines ibrutinib stromal of inhibitors ibrutinib. against in and cells. XXX rescue the driven directly and superior patient and mechanism ex-vivo stromal But multiple ibrutinib. cell of care kills are to that And FDA Thus superior of To kills data XXXX against cell isolated BTK cells primarily those a also those patient CLL kinase XXX sensitive of cells B-cell we its inhibitor, is the of CLL head inhibits Ibrutinib ibrutinib its direct the XXX shown that findings than viability. act to another from indirect loss due for FLTX malignancies. As bone samples migration greater marrow malignancy the the an activity supporting of multiple marrow the appears BTK promote To CLL killing cell studies and samples to malignancies XXX cells B-cell between range to compared signaling suppress from a more done more that and and continues in potency CLL operative head of range to the the studies cells standard inhibitors BTK and drug. vast ability signaling other ask and to retained cells operative you by BTK patients B-cell on of B-cell just $X and bone to contrast ibrutinib. in wealth BTK derived major year other the OHSU and significantly will be ibrutinib majority that team we of CLL were if must due $X like CLL ibrutinib. affect pathways. XXX then summarize and current than is grow. to development AML and freshly conditions demonstrate

Now let's and XXX that to in induced this discuss quizartinib Aptose those second of through apoptosis FLTX-ITD which cells was inhibition demonstrated research poster AML in signaling our positive XXX superior cells pre-clinical study. in the FLTX team

most and gatekeeper tested was cells patients and XXX tyrosine wall malignant potently of a in third patients, decreased tested found quizartinib, signaling. the or AML gilteritinib malignancies FLTX superior not exclusive and ibrutinib found B-cell type XXXX B-cell cell inhibited be against of that the colony phosphorylation an in inhibitors be one AML with XXX BTK innovation all more domain type have lines and non-ITD and could approximately times FLTX mutations Although in fraction B-cell kinase in express BTK FLTX mutations. to to inhibited is lines In AML to proliferation formation AML effect explained by XX which housing of crenolanib than wall FLTX-ITD patients and lesser were -- FLTX the cells domain. the

like BTK the also stromal inhibits to As cells. a cells on has cells. to nurse just is the indicated moment of ibrutinib indirect in inhibitors. bone thereby potently to considered emphasized is that it reported it lead ago pathways lead does BTK act of the to other ibrutinib to XXX can direct CLL BTK in been cells I promote not ibrutinib direct apoptotic BTK But cells CLL the from death the additional of XXX Like inhibit and the but primarily indirect CLL of Rather killing that typically killing to ibrutinib marrow those the CLL killing lead cells. XXX and and targets differentiating

So type signaling malignancies BTK up with of we the FLTX understanding aberrations. XXX. AACR XXX potent and genomic wall continue ability to And producing pathways wrap all the our of inhibit of XXX, of to advance of killing direct and target to data different types scientific multiple to mutant forms and key diverse driven by demonstrated

potentially drugs. through cells XXX were at mention quickly with data to other of here accepted kinase presentation demonstrated inhibitors and ability that abstract recently an resistance in time. XXX cluster in is to potency Stockholm the European multi look has kill we other to that EHA ability oncogenic sharing notified pan-FLTX/pan-BTK of As multiple and just more that the had at for Association also June broad animal in pathways greater would tolerated to of models or meeting to been a relative inhibitor forward like inhibition range that on we overcome to I Hematology well

studies clinical of for We that. us have are of and prepare these pursue development all to indeed eager XXX helped

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early GLP high chemistry selected studies crafted studies readily for to wedding and allows material co-milled kilogram we we agent. markerized to XXX of quantities manufacture be [ph] us First, multi human a synthetic toxicology formulation with a a that pathway the with purity,

second and this GLP have you completed kilos during GLP IND of of so to this And efficacy range product multiple dose studies We dogs. year. drug quarter finding quarter we're the in enabling again completed studies animal multiple To dogs, imminently. and substance halfway those for studies plan studies rodents remind toxicology toxicology GLP and studies, prepared second in drugs of the we planned year begin through are rodents

our then with We're plan Designation addition the IND human data indications a most we X initiate XXX for malignancies. B-cell trial second AML that track studies that timelines and emerged To in those includes to submit initiate soon as year to into Drug the patients support still thereafter. and Orphan with colleagues to received first patients remind the includes keep are you eager to designation to drive we AML on clinic we other patients plan a Phase In for trial various and XXX seek such year you as to Me the in progresses. and this will abreast of and expect we indications.

of broad may c-Myc in has and is in expression. have turn suggests now notoriously Because cell and XXX well c-Myc research Aptose's is oncogene a many regulates that end malignancies indications. oncogene inhibit growth to to certain expression. c-Myc AML a c-Myc tumor including our small application So malignancies cancer solid cancers many molecule expressed apoptosis over target inhibitor let's been difficult key APTO-XXX. across hema and cancers other in The as as it

of presented just AACR. at research a in Some that recently was poster

found damage XXX structures the are with replication force found poster quadruplex response suppress Myc trigger mechanism the in team we cells. and One in can leading and of action quadruplex certain quadruplexes programmed XXX. of Myc stabilizing of XXX XXX structure to death. BRCAX that such region BRCAX cancer those that mutated found Such heightened stabilizing Myc induction the multi promoter can DNA of certain is cancer and gene of and in cell For [indiscernible] the the demonstrated DNA research stabilizes depletion sensitivity cells of or sensitivity of The to structures. that explored cells transcription the gene in also

impaired cells far damage XXX. were mutations DNA can As functions. functions we DNA to and to as BRCAX or Indeed lead cells have the BRCAX and a a DNA cancer response found in synthetic repair drug by situation repair faulty with highly lethal studies sensitive that that

approved Myc mutation BRCAX exhibit solid hereditary acts findings with partnering to particular comparable can exhibit leverage publication Aptose now Therapeutics These recently an causes by that and in XXX cells lethality with ovarian, we prostate tumor olaparib. must in to on AML. two for for against wish and in BRCAX mechanisms online potential DNA of by lethality deficiencies. leads cancer people or XXX mention acts that and to which articles different of breast, I cancers to they that focus maintain the action a journal, we JAK The development via the Although some synthetic including that inhibitor we synthetic for new but repair cancers. XXX XXX AML and also reveal provide XXX. opportunities these Cancer inhibition must Molecular that we mechanism a indications of details AACR patients sensitivity findings cells with in mechanism remember published Hopefully FDA

our understanding made XXX to addition significant scientific we've In of development. progress -- with progress advancements XXX and

will that the for then batches the You multiple substance have manufactured drug prototype a placed on optimized CMC successfully optimized hold manufacturing, was formulation, and product we of related drug drug solubility matter. XXX clinical Since recall the process, manufacturing engineering optimized product. have and

well few AML. have we now has on questions a a this XB response and secured and response studies FDA Remember we soon plan more those accepts the we If sites and syndromes, new clinical approvals the passed from and the they stability, XXX or sterility, clinical minor supply trial of hope second of These have drug during trial and this to been studies lifted either through trial. hear lifted AML our track both phases in of submit RFB clinical the the Orphan thereafter. completed patients have or FDA immediately. quarter. participate that back fusion we been in patients Drug manufactured fitness the dosing are and tests XXX for order complete required to during a Designation dozen with of in has hold FDA clinical this of expansion drug product first demonstrate or performing During and as to with patients successfully clinical do MDS. screening more and we we product to animal have pushed GMP studies a A of as the in CMC bridging the quarter quarter then year usage. and Xb open reinitiate based escalation And if Phase have no Phase expect sites these the an is couple to XXX then begin dose for myelodysplastic hold to to early the AML With findings

So XXX patients. we're restarting eager the hopeful inhibitor the and are soon physicians of of treatment a trial for test the AML Myc clinical to

Aptose public to we insight analyst add private know another We years very and for Ms a pleased So to to Morgan the at seven. bring order Loewy's forward you number her and turn dimension financials in our both our and the Board Chow last industry. look recently of our Loewy leader keen biotechnology to business Board of Board Aptose is we know past positions that our much Members biotechnology Mr. Ms. over and an will executive working from Many companies Caroline Prudential. senior brings CFO her. to respected of with I'm and Stanley and I Ms. Directors. very accomplished before it of her for appointment as at her welcome that Caroline Loewy

milestones So more month important half and it's XXXX. to forward look a been a and we during busy

Greg. review will Officer, will Greg turn the I certainly keep now We to Financial Chief you the our results over call Mr. our for quarter. will who Chow posted.

Gregory Chow

XX.X in million XXXX. and Thank ended with you million We and cash XX.X everyone. to good the cash investments XX, at December quarter and compared Bill equivalents afternoon

first the in During XXXX. we cash our utilized approximately the of activities with quarter operating X.X compared million million of for X.X quarter

flow the the have half X.X million million release, raised subsequent This quarter. our At well year Capital. the of to in quarter disclosed $XX cash our beginning with The Aspire million was As into extended and the has was committed of second from press the Market facility we [ph] during XXXX. just X.X

the statement be for to quarter. $X.X $XXX and to same development Moving to was for and were drug $X.X activities studies General million Research XXXX. the GLP expenses quarter. million $X.X no as million for income program At expenditures period related manufacture awarded return on increased compared including primarily toxicity filing related and of Market increase drug due The range manufacture the were registration finding clinic. in increase implementation on development that compensation for to and shelf the studies stock in administrative used to announced $X.X we quarter fees million CG-XXX including GMP the supply the that the quarter the the compared is the of ATM, had facility dose primarily to in $XX well million to expense animal the increase and as previously of This and annual for professional APTO-XXX we statement the due to first revenues testing This first in expenses XXXX. and was million substance stability the

turn Finally Dr. to I for the to loss now compared or XXXX. was the X.X call $X.XX our will net $X.XX first per $X.X over per Rice. share back share or quarter in quarter million the million for Bill.

William Rice

now if could Thank introduce please questions. Greg. the open would call to like you for question. Operator the you first I


you. Thank

line Our first Newman Canaccord. from John of comes question of the

Your line is open.

John Newman

my Hey guys, good questions. Thanks afternoon. taking for

just do Bill couple am if here, seems like showed with very the we we're companies, Bill had at hear why debt one might often at sense is, just that these warrants wondering which familiar was And or structure just time? type EHA this at from any bone could lines also -- have data is, speaking? us looking I other give the more it? representative, to at have the what wondered, cell just if people wondered all then see data you you a to other but of AACR we see Greg for you don't broadly don't interesting. one I if seem Thanks. you it why general question do as for this of capital I marrow a quite you as first any more just And Just at sort sense

William Rice

you in. appreciate John, calling Thanks

I and then So, Greg the why let don’t I questions. will first answer two address other

Gregory Chow

the our No is The any actually preferred only very we or don't outstanding clean. stock, have stock. question. cap for any John structure outstanding. security is have warrants, common thanks Yeah, debt We

William Rice

was that -- XXX did of Well, you also doing it, Alright and asked meaty others now couple that question. samples we the aren’t with XXX, an marrow we've use bone about it with so with with of we have actually why done a shown reasons. it

First had Institute, Knight patient it’s set Cancer we worked Lymphoma Beat number relationship a Brian Initiative. with extraordinarily laboratory, of Leukemia We samples. get the to Dr. closely, up this Society, all Druker's of to AML difficult

then evaluated relationship with they this to a samples the these to have and bone of fresh took marrow be Center Knight these it all collect they So pull immediately. organizations together. at Cancer Then

of coming published them can't soon these ensure You first They've do this. integrity it’s TNAS paper and they on to procedure. what they in to difficult samples. another and the found paper believe had Nature and very this of Recently freeze I have away. how will technically very they in that all they difficult. But out describe studies extraordinarily It's a do

and if around tell animals you models know was mechanism cell background the put expensive it's in of means a do primary all that patients collect importance doesn't into to this and of get really get felt a agree humans. they but in the drug PK patient great guy in different difficult gets as in it it's it than these the a distributed one because and cell kill that third, what's to are to really going you We lines. my are animal those works Secondly, until to lines even to very is that thing test to because that It's system it it's samples. you're but to you cell

cost fear what range bit bridge difference potency because testing its do FLTX the to but data in between and really other of superior we killer So stark molecules. the the you you this drug lab is CLL and is And our terms of our between hope the whereas a and molecule kind our showed we're the really for in a direct Also money the against head-to-head this head ibrutinib. to all what of of it that us clinic had ibrutinib and all not. head than samples in see drug and revealed against no inhibitors ibrutinib and the of cells AML the the is us

of that it but us It's were set why hasn't gives has doing think done. sense a and you difficult I apart. So been it we to committed this

see Dr. laboratory with and June include be You is going more of also samples. that's asked in at Druker's what we to This in expect to out Stockholm. again EHA coming going to work that's

drugs. ago all -- XX pain patient patients, mentioned other had head minutes to now the marrow have samples. bone head a few against with tested we XXX had We patients we XXX tested compared have we've various over of I I CLL total think AML and actually malignancies types In

different going of more some data you'll see we're the the scatter and maps crystallography BTK in of that's a of or differentially showing and our from X-ray -- bit data heat those plots, see of to you're the drugs. that drug kinases studies to some So where other the binding some distinctly also

of broad sense you're going that's So to a see. what

for thanks the questions So John.

John Newman

you. thank Okay,


of H.C. question Thank Pantginis the Joe from next you, our line Wainwright. of is

is line open. Your

Joseph Pantginis

some the June wagons licensing for have might of Great you you others afternoon, question. deadline a good been More the full taking to the for capacity. regard of there do in have option, on ahead Hey news any a the thanks drug? and views guys, with XXX exercising curious circling that the question

William Rice

and no had that we we the wanted one as is compound, in believe were that option by the The so. to committed because Street, the we option it to to do time. it, to we're certain answer the all signal really the I the a early was On proud because do we we to reason send payment exclusive had this exercise and was we in CrystalGenomics, to is everyone decided we to agreement, said go made

might be but to question? circling Now CrystalGenomics. circling answer that get other terms not other of in reasons for they Did your companies be might that license that from

Joseph Pantginis

of That's you. data sort Bill, provide to regard since for with data of the provided, reactions ability thank you quality can to It with these additionally physician samples? AACR AACR up to sample the at would patients guess just those and of just since you regard then the patient details the translate that I helpful. clinic either all to the I does And any to thank data certainly direct ask you or specifically also are but follow

William Rice

how of the first all When Dr. out yeah, data to sees is came drugs people who compare striking. these to for lab. Druker us patients it. thanks how you the Andrea work potent literally samples. at those truth, we broad who But And such XXX docs. the at they sensitivity swathe you and against you again These the calling appreciate those Druker's can the seen tell data have the sees when shocked data a shocked Joe of it heme-onc it, well response was what Yeah, with other us Dr. and when They're Michael I versus tell are is of of it. are in, Dr.

the translates it clinic. one up hope patients does definitively into tell these not. it are into But you that what lab has no grow by so variety stand but the Many ever either cells can't of future they We also the drug in people the just involved too involved We better by different posters absorb of the other you clinic to performed has today I they in stare were data those near just it. treatment studies, all or and trying other are our physicians with I from directly in with come clinical the patients drugs, is clinical effective can whereas trials come and of the cells with the in that the are a data. how shocked trials are really you tell a at that there of these the literally number cancer had translate well

we to the as treating just will and about into as So this responses. so get great translate, data, can patients the hopefully we need we clinic possible believe feel that drug soon we see it start

effort. greatest our that's So

So thanks Joe, for appreciate questions it. the

Joseph Pantginis

You bet, thanks a lot.


Jotin Capital. The the Instructions]. from of comes Marango question ROTH [Operator line next

line is open. Your

Jotin Marango

on congrats Hi locking team, XXX. in

FLTX it's I molecule. two just the about think a have general I questions great field.

us So days their by we ago [ph] cells Daiichi our announced forced as I have to has a shown file. their relapsed you now know [ph] that few has And just Astelus told gilteritinib neither suppose hand filed these. and data. but intent was one then

this frontline think patients move you at having since positioning XXX disease, what have now you out are then do would unfit we how gilteritinib now towards quizartinib midostaurin and initially you and the it relapse in So point? chemo and thoughts fighting we about see or

William Rice

mutations at different we along. of least we continue see Well until come were it'll first failures, bridge arise drugs that to other patients some of hopefully be all a midostaurin term variety in support individual to going But long patients. do other see to that for pathways. I actually it's survival to continue believe not for approved. I a happy all believe for provide

you those mentioned forwards approval. as and quizartinib also we're seeking are move Now to see actually thrilled the gilteritinib

I particular think I much the other ITD FLTX-ITD be the drugs. you're to on with there combination also gilteritinib in heavily on much quizartinib more it's FLTX going population population are more the they're populations. in FLTX focusing looking The at think focused and

typically do tremendous is So FLTX-ITD. medical prognosis there, the as patients long, last not poor need there's a the for those

hope we patients on can they enough drugs these drugs, long stay these we for come So ALX to to hope respond along. that other can that

drugs. for then the in and that near-term by mentioned where FLTX-ITD see populations, other out So get to again us time out we the the older interest population of the ones and there tolerate of our many one the we'll the maybe we you keen of necessarily it responding. is them that battle the populations are let patients is But the cannot

has you well we the past I that wanted of And quickly been great patients we mentioned tolerated as look as far definitely and group after. a so would at in so think patients to that know those drugs possible. to Our go be

did sufficiently. answer that So

Jotin Marango

parallel and them that to I is if covalent there of of oncology. I ibrutinib on this concept a you resistant one wonder Definitely just is draw able is which the touched midostaurin the the to know other are not of and we Bill case one interesting, but and

you defines So, AML, out such at new quantify in been coming for yet are a there least have midostaurin with our in base CLL ibrutinib this resistance, population Now a is one of to resistance and able who yet. phenomenon XXX BTK thing inhibitors them is patients too,

William Rice

-- AACR, studies ASH. Yeah, presented not of a were AACR studies number excuse me, at many

been getting up of that getting in and this number talking generate to other a mutations yes, pathways the what that's that found So is that what are about arising the you're showing in midostaurin I'm mutations FLTX again also you but has are guacamole. resistance can

these but pathways that's seeing you may You enough of you effect. they lose midostaurin. And what FLTX get other are suppressive if get don't your effectively then with

it we of So is the spectrum know on a that. is all side inhibitor, one dirty kinase

but and So to some other it's that dose limiting fail on ultimately toxicity. the is the fact problem it it's have it dirty FLTX its will FLTX-ITD effect for other, The would that acts pop allow up. doesn't the pathways against

on the So you to sufficiently cells. high continue concentrations maintain cannot pressure

those variety a pathways. But in you're And with Yes, the by the patients. necessarily so got it's and failure of a up coming not resistance what ibrutinib to thing. that's you getting variety I somewhat cells. the of is seeing have for so know interesting you're of reasons from CXXXS is same

BTK. CLL bone cells the wall marrow them -- type from to cells CLL that in out excuse the a signals BTK the have that protect So CXXXS that the response me, the ibrutinib. had And then are having to mutation sending suppressing

multi essence I in molecule. is with to vivo you of trying long one it's winded cocktail to don't to it drug So escape is combination drug get ultimately drug. believe are simultaneously on the there these point why drugs. cells tear going here you. put it evolution in pathways a cells a me in have cells Well, that's got and our didn’t and on But if to other and we're way these going hit a And effectively will in these survive to number they you around any a find

Jotin Marango

Great, thank you Bill.

William Rice

you Thank Jotin.


to like am Thank back time over to you Executive Chairman, closing no the I showing and and this Dr. further at would Chief Officer turn William I President, questions. Rice, conference for remarks. the

William Rice

today joining thank and advance for hema quality support Aptose thank dedication. for our and of to to call. thank today. potential look forward Please about conclude have to advance that you opportunity we reporting employees the please We're and including again on and would at continued for and operator thank we webcast be website good work treatment and excited the posters found the us you. your recent presented back evening want Alright. We our a We note to can Everyone to interest and malignancies you our for in you you the www.aptose.com. options presentations conference


great and Ladies Everybody today's does gentlemen program. conclude this day. have a